Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.30.1 (S1 nuclease)
 3,660 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To identify factors that directly regulate the synthesis and secretion of atrial natriuretic peptide (ANP) in neuronal cells, we have developed a neuron-enriched primary culture system from fetal rat brains. A number of factors proved of importance in maintaining adequate levels of ANP secretion in such cultures: 1) cultures derived from diencephalon produced much more ANP than cultures derived from diencephalon produced with the distribution of ANP-containing cells in the rat brain; 2) brains from rats at gestational day 17 proved a better source of ANP-secreting cells than brains from rats at gestational day 16; 3) the presence of serum was required in the latter stages of the culture period to allow expression of the ANP gene; and 4) the cultures secreted more ANP when maintained at 39 C vs. 37 C. ANP mRNA transcripts in the neuron-enriched primary cultures were analyzed by S1 nuclease protection and shown to have a transcription start site similar to that employed by rat atrium and fetal hypothalamus in vivo. Dexamethasone and T3, in contrast to their stimulatory effect on ANP production in cardiocyte cultures, suppressed both the release of immunoreactive ANP and the levels of ANP mRNA in the neuron-enriched primary cultures. The cultures incorporated [35S]cysteine into immunoprecipitable ANP. HPLC analysis of 35S-labeled products in the medium revealed that, unlike neonatal cardiocyte cultures, the majority of secreted immunoreactive ANP migrated with the processed form(s) of ANP rather than the prohormone.
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PMID:Production and differential endocrine regulation of atrial natriuretic peptide in neuron-enriched primary cultures. 170 3

Murine complement protein H is encoded by a 100-kb gene on chromosome 1. A 3.2-kb fragment of the 5' flanking region of the H gene was sequenced, and two transcription start sites for this gene were identified by RNase protection and S1 nuclease analyses, each of which had upstream TATA and CAAT boxes. This region shares sequence homology with known regulatory elements, including the SV40 enhancer consensus, the Sp1 binding site, and two glucocorticoid-responsive core elements (GRE). Tissue and cell-line specificity has been examined by Northern analysis, and the 4.4-kb full-length H messenger RNA was identified in liver, kidney, spleen, thymus, liver cell line 1469, and L cells. IFN-gamma did not induce H mRNA expression in the macrophage cell line P388D.1 but had a positive effect on both the mRNA and protein levels of H in L cells. PMA, LPS, and vitamin D did not increase H mRNA levels in L cells. Pursuant to the discovery of two GRE in the 5' regulatory region of the H gene, we examined the effects of glucocorticoids on H mRNA expression. Dexamethasone (10(-7) M) was found to increase markedly the levels of H mRNA and protein after 24 h of incubation, and the effect on the mRNA was detectable by 30 min. The fact that H is a down-regulator of complement activation is consistent with the known immunosuppressive role of glucocorticoids. To our knowledge, this is the first time that dexamethasone has been shown to increase the levels of a complement protein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analysis of complement factor H mRNA expression: dexamethasone and IFN-gamma increase the level of H in L cells. 253 12

The promoter region of the human insulin-receptor (HINSR) gene was isolated from a human chromosome 19 bacteriophage library. With S1 nuclease mapping and primer-extension analysis, we identified multiple transcription-initiation sites. Dexamethasone, a known inducer of HINSR transcription, enhanced transcription of all major transcription-initiation sites. DNA sequence analysis indicated that the HINSR promoter has neither a TATA box nor a CAAT box. The HINSR promoter region contains six GGGCGG sequences that may be binding sites for the transcription factor Sp1. In addition, there were three TCCC sequences that were putative promoter regulatory regions. The HINSR gene promoter has structural similarity to the epidermal growth factor receptor gene promoter and has some features of the promoter of the meglutol (hydroxymethylglutaryl, HMG) CoA reductase gene and the early promoter of simian virus 40.
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PMID:Sequence and analysis of promoter region of human insulin-receptor gene. 341 Jan 65

Highly purified recombinant human tumor necrosis factor (TNF) was found to induce interleukin 1 (IL 1) production in diploid human FS-4 fibroblasts. Demonstration of IL 1 activity was based on the ability of TNF-treated FS-4 cells, subsequently fixed with formaldehyde, to stimulate thymocyte proliferation in the presence of phytohemagglutinin. Incubation of FS-4 cells with the optimal dose of TNF (10 ng/ml) resulted in a marked increase in [3H] thymidine uptake by thymocytes co-cultured with formaldehyde-fixed FS-4 cells. Induction of this apparently membrane-associated IL 1 (MA-IL 1) activity was demonstrable at 6 hr and reached a plateau after 48 hr of incubation with TNF. FS-4 cells did not secrete soluble IL 1 in response to TNF. Dexamethasone suppressed the synthesis of TNF-induced MA-IL 1. A monoclonal antibody specific for TNF neutralized MA-IL 1 induction, indicating that the induction is due to TNF, and not to a contaminant in the TNF preparation. The ability of TNF to induce IL 1 synthesis in FS-4 fibroblasts at the transcriptional level was confirmed by S1 nuclease protection assay. Cytoplasmic RNA from uninduced FS-4 cells contained no demonstrable RNA hybridizing with a human IL 1-alpha cDNA probe and low levels of RNA hybridizing with an IL 1-beta cDNA. Induction with TNF resulted in the appearance of IL 1-alpha mRNA and a very significant increase in IL 1-beta mRNA, indicating that TNF induces the synthesis of both IL 1-alpha and IL 1-beta in FS-4 cells.
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PMID:Induction of membrane-associated interleukin 1 by tumor necrosis factor in human fibroblasts. 349 60